The aim of this project is to develop a small animal model of cardiac dilatation and congestive failure induced by chronic alchohl ingestion. Once the model is developed we will use it to test the hypothesis that autonomic mediators and changes in cardiac cell responsiveness are important in the development of alcohol induced cardiomyopathy. This will be accomplished by determining the effect of chronic alcohol ingestion on the maximum concentration of Beta and muscarinic receptors and binding affinity for the labelled antagonist and the agonists, isoproterenol and carbachol in the presence of GTP, in the heart. We will then test the effects of isoproterenol and carbachol on sinoatrial rate, atrial contractility and ventricular contractility in isolated tissue preparations made from the hearts of alcohol treated rats. We will further study the cellular level responses of these cardiac tissues by quantitating the adenylate cyclase response to Beta and muscarinic stimulation. We will measure phospholipid methylation and Na, K/ATPase activity by quantitating [3H]-Ouabain binding to the cardiac glycoside receptor in these tissues. The rationale for these studies in the chronic alcohol model is that an increase in the work of the heart which can be caused by increases in the rate of beating, contractility, preload, and afterload may lead to dilatation, hypertrophy and failure. These effects can all be precipitated by altered responsiveness to beta and muscarinic agents. This study will determine if an altered responsiveness which is conducive to the development of failure is present in the hearts of rats which chronically consume alcohol.